Exam 1 - infectious diseases and abx

Question 1

What is the etiologic agent of feline infectious peritonitis?

Answer 1

Feline coronavirus (+ssRNA, enveloped)

Question 2

What are the two presentations of feline coronavirus?

Answer 2

GI disease and FIP

Question 3

What is the theory of FIP pathogenesis (what makes it different from standard FeCoV infection)?

Answer 3

Mutation in FeCoV strain allows for macrophage tropism

Question 4

What signalment is typical of FIP?

Answer 4

3 months - 3 years
purebred cats
overcrowded/stressful environment

Question 5

How is FeCoV transmitted?

Answer 5

Oronasal exposure to feces/fomites

Question 6

Describe the pathogenesis of FIP in the body.

Answer 6

Macrophage infection –> systemic pyogranulomatous vasculitis
Wet form associated with inadequate CMI –> exudation of plasma proteins
Dry form associated with partially protective CMI –> granuloma/pyogranuloma formation

Question 7

Describe the concept of “antibody dependent enhancement” (ADE) in relation to FIP

Answer 7

Sub-neutralizing antibodies accelerate the disease process

M0s bind to Ab-virus complex > more viral infection of macrophages

Question 8

What clinical signs are associated with FIP?

Answer 8

Vague: lethargy, anorexia, weight loss, chronic fever
Wet-specific: high protein fluid accumulation in body cavities
Dry-specific: pyogranulomatous lesions in eyes, CNS, LNs

Question 9

How is FIP diagnosed?

Answer 9

Chem - hyperglob and hypoalb (alb:glob <4 highly predictive), hyperbili
Polyclonal gammopathy
*Immunohistochem is GS, but can only be done post-mortem
*IFA serum ELISA is GS for FeCoV Ab detection but does NOT predict FIP
rt-PCR - sensitive for FIP with effusion sample

Question 10

How is FIP treated?

Answer 10

Prednisone (immunosuppressive dose) - NOT curative

Intracavitary dexamethasone for effusions

Question 11

How is FIP prevented?

Answer 11

Test queen before kittens born - if + remove kittens at 4-6 weeks
Vaccination is non-core and not recommended

Question 12

What is the prognosis for FIP?

Answer 12

Poor (9-38 days)

NPIs: hyperbili, lymphopenia, large volumes of effusion

Question 13

What is the etiology of infectious canine hepatitis?

Answer 13

Canine adenovirus 1 (CAV-1) (dsDNA, non-enveloped)

Question 14

Why is infectious canine hepatitis rarely seen in the US?

Answer 14

Cross vaccination with CAV-2

Question 15

How is infectious canine hepatitis transmitted?

Answer 15

oronasal with urine contact

Question 16

What is the pathogenesis and CS associated with infectious canine hepatitis?

Answer 16

Infection of hepatocytes and endothelial cells
Blue eye
Glomerulonephritis
Icterus

Question 17

How is canine distemper virus transmitted?

Answer 17

Aerosol, respiratory secretions

Question 18

What signalment is typical with canine distemper virus?

Answer 18

Puppies 3-6 months (d/t loss of maternal Ab)

Question 19

Describe the pathogenesis of canine distemper.

Answer 19

Local tissue M0 infection > lymphoid infection and viremia > *epithelial cell and CNS infection
Variable immune response may lead to viral persistence (hard pad dz, optic neuritis, KCS, etc.), or widespread tissue infection (GI, genitourinary, respiratory, skin, and CNS infection)

Question 20

What three presentations of CNS disease are seen with canine distemper?

Answer 20

1. Acute CDV encephalitis (acute, non-inflammatory demyelination in puppies d/t viral replication)
2. Subacute and chronic (demyelinating immune reaction in older dogs, not associated with viral replication)
3. “Old dog encephalitis” (chronic active and progressive inflammation of cerebrum/brainstem grey matter, occurs weeks to years after infection)

Question 21

What clinical signs are associated with canine distemper?

Answer 21

Cough, runny nose, respiratory distress
Seizures
Diarrhea, vomiting, tenesmus, intussuseption (ddx parvo)
Chorioretinitis (gold medallion lesions)
Nasal and digital hyperkeratosis
Progressive encephalitis with repetitive motions

Question 22

How is canine distemper diagnosed?

Answer 22

Primarily clinical suspicion!
ELISA IgM - acute cases
ELISA IgG - past or present infeciton or vaccination

Question 23

How is canine distemper treated/prevented?

Answer 23

No treatment.

Vaccination VERY effective!

Question 24

How is rabies transmitted?

Answer 24

Saliva - salivary shedding can occur before CS apparent!

Question 25

Describe the pathogenesis of rabies.

Answer 25

Enters peripheral nerves and replicates locally > spreads passively by intra-axonal flow Incubation: dogs and cats (1-6 months), humans (1-12 months) Enters spinal cord/brainstem ipsilateral to bite > spread to contralateral side > ascends bilaterally to forebrain > progressive LMN disease Spread to acinar cells of salivary gland

Question 26

Describe the clinical phases of rabies

Answer 26

1. Prodromal (CNS viral spread) - mood change, variable fever, pupils dilated, pruritis 2. Furious (forebrain involvement) - common in cats - hyperesthesia, photophobia, aggression, seizures 3. Paralytic - common in dogs - ascending flaccid paralysis 4. Death - within 2-4 days of clinical onset

Question 27

How is rabies diagnosed?

Answer 27

Clinical suspicion - any animal that suddenly develops profound behavioral changes and/or LMN paralysis Histopath: negri bodies and perivascular cuffing *Direct fluorescent Ab test

Question 28

What specimens should be sent in suspected rabies cases? How should they be preserved?

Answer 28

Hippocampus, cerebellum, medulla oblongata | Fresh or refrigerated (NOT frozen or in formalin)

Question 29

A dog who is up-to-date on the rabies vax comes to you after being bitten by a racoon. What do you tell the owners regarding rabies risk/protocol?

Answer 29

Revaccinate | 45 day observation period

Question 30

A cat who was never vaccinated for rabies comes to you after being bitten by a bat. What do you tell the owners regarding rabies risk/protocol?

Answer 30

Vaccinate | 180 day observation period

Question 31

Mrs. Hutchinson's daughter was bitten by their darling dog, Fluffy, yesterday. Fluffy is healthy but not UTD on the rabies vax and Mrs. H doesn't want to euthanize. What do you tell her regarding rabies risk/protocol?

Answer 31

DO NOT vaccinate | 10 day observation period

Question 32

How is Clostridium botulinum transmitted?

Answer 32

Food-borne ingestion of preformed toxin

Question 33

Describe the pathogenesis of C. botulinum infection.

Answer 33

Toxin absorbed in small intestines > lymphatics and bloodstream > neural intoxication: 1. toxin binds to cell surface receptors 2. internalization of toxin into endosomal compartments 3. membrane translocation 3. enzymatic cleavage of SNARE proteins (important in release of Ach > paralysis at NMJ)

Question 34

What clinical signs are consistent with C. botulinum?

Answer 34

Ascending flaccid paralysis - though mentally alert and tail wag maintained!

Question 35

List some ddx for ascending flaccid paralysis:

Answer 35

1. C. botulinum 2. Polyradiculoneuritis (Coonhound paralysis) - muscle wasting and hyperesthesia 3. Tick paralysis (less CN involvement) 4. Myasthenia gravis (will be episodic)

Question 36

How is C. botulinum infection diagnosed?

Answer 36

Clinical signs | Confirmed by finding toxin in serum/feces/vomit/food sample (mouse inoculation test)

Question 37

How is C. botulinum treated?

Answer 37

``` Equine antitoxin (not effective once bound to the nerve) Supportive therapy ```

Question 38

What is the prognosis for C. botulinum infection?

Answer 38

Good! Complete recovery in 14-21 days barring secondary infection or respiratory failure

Question 39

What is the etiology of tetanus?

Answer 39

Clostridium tetani

Question 40

What are the two tetanus toxins? Which causes clinical signs?

Answer 40

Tetanospasmin - CS! | Tetanolysin

Question 41

What are the three forms of tetanus?

Answer 41

1. Localized disease 2. Generalized disease - spastic paralysis 3. Cranial nerve tetanus - risus sardonicus, trismus, protrusion of 3rd eyelid, laryngeal spasm

Question 42

Describe the pathogenesis of tetanus.

Answer 42

Wound contaminated with C. tetani spores > anaerobic environment promotes germination > toxin attaches to peripheral nerves > migrates retrograde to CNS > prevents release of inhibitory neurotransmitters (irreversibly!) > spastic paralysis

Question 43

How is tetanus treated?

Answer 43

Antitoxin - risk of anaphylaxis PenG, metronidazole (IV) Clean/debride wound Supportive care - quiet, non-stimulating environment

Question 44

What is the prognosis for tetanus cases?

Answer 44

Complete recovery expected if they can survive the initial period May take up to 2 weeks before improvement observed Full recovery within 60 days

Question 45

Which antibiotics are concentration dependent?

Answer 45

Metronidazole (nitroimidazoles) Fluoroquinolones Aminoglycosides Glycopeptides (Vancomycin)